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Stimulation of nitric oxide synthase in cerebral cortex due to elevated partial pressures of oxygen: An oxidative stress response
Journal of neurobiology, 2002-05, Vol.51 (2), p.85-100
Thom, Stephen R.
Bhopale, Veena
Fisher, Donald
Manevich, Yefim
Huang, Paul L.
Buerk, Donald G.
2002
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Thom, Stephen R.
Bhopale, Veena
Fisher, Donald
Manevich, Yefim
Huang, Paul L.
Buerk, Donald G.
Titel
Stimulation of nitric oxide synthase in cerebral cortex due to elevated partial pressures of oxygen: An oxidative stress response
Ist Teil von
Journal of neurobiology, 2002-05, Vol.51 (2), p.85-100
Ort / Verlag
New York: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2002
Quelle
Wiley Blackwell Single Titles
Beschreibungen/Notizen
The purpose of this investigation was to determine the impact of elevated partial pressures of O2 on the steady state concentration of nitric oxide (•NO) in the cerebral cortex. Rodents with implanted O2‐ and •NO‐specific microelectrodes were exposed to O2 at partial pressures from 0.2 to 2.8 atmospheres absolute (ATA) for up to 45 min. Elevations in •NO concentration occurred with all partial pressures above that of ambient air. In rats exposed to 2.8 ATA O2 the increase was 692 ± 73 nM (S.E., n = 5) over control. Changes were not associated with alterations in concentrations of nitric oxide synthase (NOS) enzymes. Based on studies with knock‐out mice lacking genes for neuronal NOS (nNOS) or endothelial NOS (eNOS), nNOS activity contributed over 90% to total •NO elevation due to hyperoxia. Immunoprecipitation studies indicated that hyperoxia doubles the amount of nNOS associated with the molecular chaperone, heat shock protein 90 (Hsp90). Both •NO elevations and the association between nNOS and Hsp90 were inhibited in rats infused with superoxide dismutase. Elevations of •NO were also inhibited by treatment with the relatively specific nNOS inhibitor, 7 nitroindazole, by the ansamycin antibiotics herbimycin and geldanamycin, by the antioxidant N‐acetylcysteine, by the calcium channel blocker nimodipine, and by the N‐methyl‐D‐aspartate inhibitor, MK 801. Hyperoxia did not alter eNOS association with Hsp90, nor did it modify nNOS or eNOS associations with calmodulin, the magnitude of eNOS tyrosine phosphorylation, or nNOS phosphorylation via calmodulin kinase. Cerebral cortex blood flow, measured by laser Doppler flow probe, increased during hyperoxia and may be causally related to elevations of steady state •NO concentration. We conclude that hyperoxia causes an increase in •NO synthesis as part of a response to oxidative stress. Mechanisms for nNOS activation include augmentation in the association with Hsp90 and intracellular entry of calcium. © 2002 Wiley Periodicals, Inc. J Neurobiol 51: 85–100, 2002
Sprache
Englisch
Identifikatoren
ISSN: 0022-3034
eISSN: 1097-4695
DOI: 10.1002/neu.10044
Titel-ID: cdi_proquest_miscellaneous_71571198
Format
–
Schlagworte
Animals
,
Antioxidants - pharmacology
,
cerebral blood flow
,
Cerebral Cortex - enzymology
,
Cerebral Cortex - physiology
,
Enzyme Activation - drug effects
,
Enzyme Activation - physiology
,
heat shock protein 90
,
hyperbaric oxygen
,
Hyperbaric Oxygenation - methods
,
Hyperbaric Oxygenation - statistics & numerical data
,
Isoenzymes - deficiency
,
Isoenzymes - metabolism
,
Male
,
Mice
,
Mice, Knockout
,
MK 801
,
Nitric Oxide - antagonists & inhibitors
,
Nitric Oxide - physiology
,
Nitric Oxide Synthase - antagonists & inhibitors
,
Nitric Oxide Synthase - deficiency
,
Nitric Oxide Synthase - metabolism
,
Nitric Oxide Synthase Type I
,
Oxidative Stress - physiology
,
Oxygen - metabolism
,
Partial Pressure
,
Precipitin Tests
,
Rats
,
Rats, Wistar
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